In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERSNo. [redacted]VOctober 16, 2008

Reissued redacted: October 31, 2008To be Published

* * * * * * * * * * * * * * * * * * * * * * * * * * * * *JANE DOE/23, * * Petitioner, * *

v. * Entitlement; hepatitis B vaccine; * visual difficulties one monthSECRETARY OF THE DEPARTMENT OF * later and MS diagnosis threeHEALTH AND HUMAN SERVICES, * months later *

Respondent. ** * * * * * * * * * * * * * * * * * * * * * * * * * * * *Clifford J. Shoemaker, Vienna, VA, for petitioner.Richard F. Topping, Washington, DC, for respondent.

MILLMAN, Special Master

RULING ON ENTITLEMENT1

Vaccine Rule 18(b) states that all decisions of the special masters will be made1

available to the public unless they contain trade secrets or commercial or financial informationthat is privileged and confidential, or medical or similar information whose disclosure would e aclearly unwarranted invasion of privacy. When such a decision or designated substantive order isfiled, petitioner has 14 days to identify and move to delete such information prior to thedocument’s disclosure. If the special master, upon review, agrees that the identified material fitswithin the banned categories listed above, the special master shall delete such material frompublic access. On October 30, 2008, petitioner moved to redact her name from the decision. Theundersigned grants her motion.

Petitioner filed a petition on May 17, 1999, under the National Childhood Vaccine Injury

Act, 42 U.S.C. §300aa-10 et seq., alleging that she received hepatitis B vaccine on November 12,

1992, December 18, 1992, and May 25, 1993, and experienced an adverse reaction.

Petitioner had optic neuritis and has multiple sclerosis (MS). Onset is the issue of the

case. A hearing was held on June 17, 2008. Testifying for petitioner was Dr. Carlo Tornatore.

Testifying for respondent was Dr. Aaron E. Miller.

This is one of the cases affected by the undersigned’s rulings in the Omnibus proceeding

dealing with hepatitis B vaccine and demyelinating diseases such as transverse myelitis (TM),

Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating disease (CIDP), and

multiple sclerosis (MS). The undersigned held that hepatitis B vaccine can cause these diseases

if the onset is between three days and one month based on the Omnibus testimony of petitioners’

expert Dr. Vera Byers and respondent’s expert Dr. Roland Martin. Stevens v. Secretary of HHS,

No. 99-594, 2006 WL 659525, at *12, *15 (Fed. Cl. Feb. 24, 2006). 2

Recently, in Pecorella v. Secretary of HHS, No. 04-1781V, 2008 WL 4447607 (Fed. Cl.

Spec. Mstr. Sept. 17, 2008), the undersigned ruled that an appropriate onset could be up to two

months.

FACTS

Stevens v. Secretary of HHS, No. 99-594, 2006 WL 659525 (Fed. Cl. Spec. Mstr. Feb.2

24, 2006) (hepatitis B vaccine caused TM; onset was12 or 13 days after first vaccination withrecovery; onset of TM was one week after second vaccination); Gilbert v. Secretary of HHS, No.04-455V, 2006 WL 1006612 (Fed. Cl. Spec. Mstr. Mar. 30, 2006) (hepatitis B vaccine causedGBS and CIDP; onset was 21 days after second vaccination); Werderitsh v. Secretary of HHS,No. 99-310V, 2006 WL 1672884 (Fed. Cl. Spec. Mstr. May 26, 2006) (hepatitis B vaccinecaused MS; onset was one month after second vaccination); Peugh v. Secretary of HHS, No. 99-638V, 2007 WL 1531666 (Fed. Cl. Spec. Mstr. May 8, 2007) (hepatitis B vaccine caused GBSand death; onset of GBS was eight days after fourth vaccination).

2

Before the Vaccinations

Petitioner was born on March 13, 1960.

On September 18, 1987, petitioner went to St. Elizabeth Hospital Medical Center,

complaining of back pain which began the prior day after she was lifting at work. She also had

numbness. Med. recs. at Ex. 7, p. 5. Dr. J.P. Brown’s impression was thoracic spine strain and

he advised petitioner to avoid heavy lifting. Med. recs. at Ex. 7, p. 7. She had some numbness

over the right shoulder and leg region but denied weakness in the upper or lower extremities.

She was treated in the recent past for episodes of back pain. Back examination revealed minimal

spasm amid the thoracic spine, particularly on the right. There were no objective sensory or

motor findings. She walked without difficulty. Id.

On May 1, 1989, petitioner complained of right knee pain. Med. recs. at Ex. 7, p. 2.

On September 4, 1990, petitioner was diagnosed with right knee tendinitis. Id. She went

to the Emergency Department of Lafayette Home Hospital. Two years previously, she had fluid

behind the right knee but no problems since. She complained of pain for two days behind the

right knee which radiated to the thigh and the calf. She had intermittent sharpness with tingling

in her right toes. She had no swelling. She had a burning sensation in her foot. She had good

range of motion. The diagnosis was tendinitis in the right knee. Med. recs. at Ex. 7, p. 9.

After the Vaccinations

Petitioner received hepatitis B vaccinations on November 12, 1992, December 18, 1992,

and May 25, 1993. Med. recs. at Ex. 2, p. 2.

3

On June 28, 1993, one month after the third hepatitis B vaccination, petitioner saw Dr.

Nicholas F. Hrisomalos, a retina specialist, for photopsias and film that she had noted in her3

right eye over the prior week. Examination showed vitreous floaters in each eye with an annulus4

appearing on the right. There was no vitreous hemorrhage or pigment. The macula in the right

eye had some conspicuous pigmentary changes and drusen. Peripheral retinal examination of5

the left eye showed peripheral cystoid degeneration but no significant retinal tear, hole, or

detachment. In the right eye was a patch of lattice degeneration inferiorly and early developing

traction inferiorly temporally. Superiorly, there was another area of light without traction. Dr.

Hrisomalos’s impression was high myopia with posterior vitreous detachment and some

peripheral retinal changes in the right eye. No treatment was recommended. Med. recs. at Ex. 4,

p. 4.

On August 2, 1993, petitioner returned to Dr. Hrisomalos, complaining that the film,

sparklers, flashing lights, and distorted vision were just the same or worse. Her headaches were

less and her vision was still slightly blurred but not worse. She reported some possible changes

in her color vision. Angiography was performed which showed a small area in the macula

inferior nasally which looked like a small laquer crack. There was no evidence of subretinal

Photopsia is “an appearance as of sparks or flashes due to retinal irritation.” Dorland’s3

Illustrated Medical Dictionary, 30 ed. (2003) at 1431.th

An annulus is “a ring or ringlike structure....” Dorland’s Illustrated Medical Dictionary,4

30 ed. (2003) at 93.th

Drusen (German for “bumps”) are “hyaline excrescences in Bruch’s membrane (lamina5

basalis choroideae); they usually result from aging, but sometimes occur with pathologicconditions....” Dorland’s Illustrated Medical Dictionary, 30 ed. (2003) at 565. Basal lamina ofth

choroid is “the transparent inner layer of the choroid, which is in contact with the pigmentedlayer of the retina.” Id. at 993.

4

neovascularization or other change. He called petitioner and recommended she check her central

vision daily and report any distortion, and check her peripheral vision for any sign of retinal

detachment. Med. recs. at Ex. 4, p. 3.

On September 21, 1993, at 7:54 p.m., petitioner went to Lafayette Home Hospital

Emergency Department, complaining of pain in her medial right leg proximal and distal to her

knee, which started at noon that day and was tender to the touch. She was at work and tried to

walk the pain out for about 20 minutes. The pain went away and she felt lightheaded as if she

would pass out, but she did not. She came to the hospital and felt better. She had a history of

phlebitis in her right leg. Her left inner thigh felt like it was on fire. On examination, her gait

and squat were normal. There was no heat or redness on either leg. She was diagnosed with a

vasovagal episode and leg pain. Med. recs. at Ex. 8, p. 31. 6

On September 22, 1993, Dr. Anna L. Welch worked petitioner into her schedule because

of pain in petitioner’s left leg with numbness. She had had trouble with both legs intermittently

for years and had a history of phlebitis. She had pain and burning in the medial left thigh. She

had shortness of breath the prior night and went to the emergency room. Her deep tendon

reflexes were normal. Her left thigh was tender to palpation but not red or warm. Med. recs. at

Ex. 6, p. 14.

On September 23, 1993, Dr. Welch noted that petitioner could return to work. Id.

Vasovagal attack is “a transient vascular and neurogenic reaction marked by pallor,6

nausea, sweating, bradycardia, and rapid fall in arterial blood pressure which, when below acritical level, results in loss of consciousness and characteristic electroencephalographic changes. It is most often evoked by emotional stress associated with fear or pain.” Dorland’s IllustratedMedical Dictionary, 30 ed. (2003) at 178.th

5

On September 27, 1993, Dr. Welch noted petitioner’s legs were numb and her feet cold.

She had difficulty ambulating and slid down a hill one week previously on her right buttock. She

had no deep tendon reflex on the right. Her left leg was cooler than her right leg. Id.

On September 29, 1993, petitioner underwent a left lumbar spinal MRI, which was

normal except for mild scoliosis and early dehydration of the L5-S1 intervertebral disc due to

age. Med. recs. at Ex. 1, p. 13.

On September 30, 1993, she saw Dr. Michael A. Sermersheim, a neurologist, on referral

from Dr. Welch, complaining of clumsiness, numbness, and weakness of her lower extremities

for about 10 days. Med. recs. at Ex. 1, p. 17. Initially she felt it more in the left lower extremity,

but she very quickly started experiencing the sensation in both lower extremities. Id. She denied

any recent illnesses. Id. She had never experienced this sensation before in her life. She had

never had any other transient neurologic deficits, specifically no visual disturbances, numbness

and tingling in the upper extremities, or personality changes. She was basically healthy and had

no significant health problems in the past. Id.

On October 1, 1993, petitioner underwent a nerve conduction study and right peroneal F-

wave latency test. Petitioner had complained of 10 days of numbness and tingling in her lower

extremities. The study was essentially normal. Dr. Sermersheim stated she had mild delay in the

posterior tibial distal latency which was of uncertain clinical significance. The study results did

not suggest peripheral neuropathy or Guillain-Barré syndrome. Med. recs. at Ex. 8, p. 27.

On October 14, 1993, petitioner underwent a brain MRI, which was abnormal due to

increased T2 signal in the posterior parietal white matter bilaterally and in the medial left

brachium pontis. The primary consideration would be MS. Med. recs. at Ex. 1, p. 15.

6

On October 20, 1993, Dr. Sermersheim wrote a letter to Dr. Welch to update her on

petitioner. Petitioner’s lumbar puncture and brain MRI were most consistent with the diagnosis

of MS. Med. recs. at Ex. 1, p. 3.

On October 13, 1994, petitioner saw Dr. Catherine I. Hatvani who, in reviewing

petitioner’s history, stated that petitioner had MS with some involvement of the lower

extremities and not much involvement of her vision or upper extremities. Med. recs. at Ex. 16,

p. 27. She had headaches associated with tension. She had tension and pain in the back of the

neck associated with work-related tension. Id.

Five years later, on December 17, 1999, petitioner saw Dr. Hamid S. Hamdi, a

neurologist, complaining of sudden onset of loss of vision in her left eye, decreased visual acuity,

and burning sensations and hyperesthesias in both lower extremities. On examination, Dr.

Hamdi did not see any relative afferent pupillary defect. The fundi appeared normal on the left

side. The right side showed some atrophy. Petitioner had a patchy loss of sensation in all

extremities. Her strength, tone, and deep tendon reflexes were normal. His impression was left

optic neuritis. Med. recs. at Ex. 17, p. 10.

Later on December 17, 1999, at Lafayette Home Hospital, Dr. Hamdi wrote a history and

physical examination of petitioner, stating that petitioner had a history of MS diagnosed in 1993

when she presented with right optic neuritis from which she had partially recovered. She came to

his office, complaining of sudden onset of decreased vision in the left eye which started the day

before. Dr. Hamdi saw petitioner in his office that afternoon and she was admitted to Lafayette

Home Hospital, Inc. for IV steroid treatment. Petitioner had decreased visual acuity in both eyes

7

with left pupillary defect. She had pallor in the right fundus and a normal fundus in the left side.

He diagnosed petitioner with acute left optic neuritis. Med. recs. at Ex. 17, p. 16.

On January 25, 2000, petitioner underwent another brain MRI which was compared to her

prior MRI of October 14, 1993. Dr. Douglas M. Dunco’s impression was interval decrease in the

left bracium pontis signal abnormality with stable deep white matter foci of signal abnormality in

the parietal regions and with new lesions in the centrum semiovale bilaterally, with an acute

lesion in the temporooccipital region. The findings were consistent with MS. Med. recs. at Ex.

17, p. 15.

On September 29, 2000, petitioner suffered cardiac arrest and associated hypoxia with

memory and other cognitive difficulties. Med. recs. at Ex. 12, p. 24.

Other Submitted Material

Petitioner filed Ex. #22, an article entitled “Retinal Venous Sheathing and the Blood-

Retinal Barrier in Multiple Sclerosis,” by M.K. Birch, et al., 114 Arch Ophthalmol 34-39 (1996).

There is a well-recognized association between retinal venous sheathing and MS. Id. at 34. The

inflammatory nature of some of the retinal venous changes associated with MS has been shown

by disruption of the blood-retinal barrier (BRB) in a few patients. Id. Intracranial venulitis in

white matter in or between demyelinated plaques in MS may be associated with retinal venous

sheathing and have a common cause. Id.

Petitioner filed Ex. #23, which is an excerpt from a text called Neuro-Ophthalmology.

Diagnosis and Management, eds. Liu, et al., “Inflammatory Optic Neuropathies,” pp. 128, 129.

The authors state, at 128:

8

The inflammatory optic neuropathies represent a heterogeneousgroup of conditions characterized by acute or subacute, oftenpainful vision loss that results from inflammation of the opticnerve. . . . The term optic neuritis has come to have an even morespecific implication: inflammatory optic neuropathy thataccompanies demyelinating disease. . . . These processes may beimmune mediated, granulomatous, or infectious. . . . In manypatients optic neuritis is the heralding manifestation of multiplesclerosis.

The authors continue, at 128-29:

Vision loss is rapid in onset, generally being recognized over aperiod of hours to a few days. . . . Reduced color vision invariablyaccompanies the vision loss in optic neuritis. . . . Characteristicpain precedes the vision loss by a few days and is present in themajority of patients. . . . Global tenderness and worsening of painon eye movements are typical. The exact origin of the pain isunknown but presumably pain is the result of the pulling on thedura (in contact with the inflamed nerve) by the eye muscle origin .. . . Phosphenes or flashing lights described by patients with opticneuritis generally take a variety of forms, including lights, sparkles,and shifting squares. . . . These symptoms were present in 30% ofpatients . . . . Uhthoff’s symptom is transient visual obscurationassociated with elevation in body temperature. . . . Vision lossgenerally takes the form of blurring, greying, or reduced colorvision . . . . Patients with optic neuritis almost always have somevisual field loss.

Petitioner filed Ex. #24, an excerpt from Principles and Practice of Ophthalmology, 2nd

ed., Vol. 5, eds. Albert & Jakobiec, pp. 4120-23. The authors list clinical signs of optic neuritis

on p. 4120 as: reduced visual acuity at near and far distance, dyschromatopsia (abnormal color

vision), impaired contrast sensitivity, reduced stereoacuity, general depression of the visual field,

afferent pupillary defect, and hyperemia and acute swelling of the optic disc. Abnormal color

vision occurs in patients with acute and recovered optic neuritis. Id. The authors state, “Color

vision defects are highly sensitive indicators of a previous attack of optic neuritis.” Id. at 4121.

9

“In acute optic neuritis, the cardinal field defect is a widespread depression of sensitivity, which

is particularly pronounced centrally as a central scotoma.” Id. at 4123. A unilateral relative

afferent pupillary defect is present in 44-76% of patients with acute optic neuritis. Id.

Petitioner filed Ex. #25, an article entitled “Retinal Venous Sheathing in Optic Neuritis.

Its Significance for the Pathogenesis of Multiple Sclerosis,” by S. Lightman, et al., 110 Brain

405-14 (1987). The authors found vascular abnormalities and/or cells in the media of one-

quarter of patients presenting with their first attack of an apparently isolated optic neuritis which

the authors considered predictive in assessing the risk of developing clinically expressed MS. Id.

at 405-06, 411. They thought it possible that the primary events leading to demyelination

occurred at the vascular endothelium. Id. at 412.

TESTIMONY

Dr. Carlo Tornatore, a neurologist, testified for petitioner. Tr. at 5. He is the director of

the MS Center at Georgetown. Tr. at 7. On June 28, 1993, about a month after petitioner’s third

hepatitis B vaccination, petitioner had flashing lights or photopsias and a film over her right eye.

Tr. at 12. The timing is appropriate for the onset of an autoimmune response to a vaccination.

Id. Dr. Nicholas F. Hrisomalos wrote that petitioner also had headache, sparkles, and the

sensation of looking through a screen. Id. She said these symptoms began about a week earlier,

putting onset at June 21, 1993. Id.

In a follow up visit on August 2, 1993, petitioner reported some possible change in her

color vision. Tr. at 13. This would mean color loss. Tr. at 14. Dr. Hrisomalos was a retinal

specialist. Id. He was looking only at petitioner’s retina. Id. Petitioner’s change in her color

vision may have been color loss. Id. Dr. Tornatore emphasized four symptoms about which

10

petitioner complained to Dr. Hrisomalos: flashing lights (sparkles or photopsias), visual

obscuration (the screen in front of her eyes), pain (headache), and loss of or changing color. Tr.

at 17-18.

Phosphenes or flashing lights are present in 30 percent of patients with optic neuritis. Tr.

at 18-19. They could also occur in neuroretinitis. Tr. at 19. Dr. Tornatore thinks that Dr.

Hrisomalos did not diagnose petitioner with optic neuritis because, being a retinal specialist, he

thought there was something wrong with her retina. Id.

To find out if petitioner’s symptom of headaches really was pain in her eye, Dr. Tornatore

questioned her the day before the hearing. Tr. at 20. But petitioner did not recall where the pain

was. Id. Dr. Tornatore stated that Dr. Hrisomalos, being a retina specialist, did not describe

petitioner’s pupils or her optic nerve to say whether they were normal or abnormal in his written

notes and diagram. Tr. at 23. He spent a lot of time looking at the periphery of petitioner’s

retina and found changes which could be old in someone with myopia. Id.

Someone with optic neuritis would have an afferent pupillary defect. Tr. at 23-24. Dr.

Hrisomalos recognized the complaint of decreased vision and color vision and did a fluorescein

angiogram. Tr. at 28. This helps see the blood vessels in the back of the eye. Id. Petitioner had

a small area in the macular region inferior nasally which seemed like a small laquer crack, i.e., a

little break in a blood vessel or small, leaky vessel. Tr. at 29. In optic neuritis, there is some

focus leakage out of the blood vessel of the eye. Tr. at 31. Dr. Hrisomalos did not indicate if the

leak were in a vein or an artery. Id. Leaky blood vessels are well recognized in someone with

optic neuritis. Id.

11

Six years after petitioner’s first symptoms, Dr. Hamdi at Lafayette Home Hospital notes

that petitioner had right optic neuritis in 1993 from which she had partially recovered. Tr. at 33-

34. This was after she had been diagnosed with MS. Tr. at 34. She then had problems with her

left eye. Id. Dr. Hamdi wrote petitioner had right fundal pallor. Id. Normally, it is yellowish.

Id. Pallor is a hallmark of someone with atrophy of the optic nerve. Tr. at 34-35. Optic neuritis,

but not retinal detachment, would cause pallor of the optic nerve. Tr. at 35. In Dr. Hamdi’s

letter of December 17, 1999, he states that petitioner’s right fundus showed some atrophy,

meaning her right optic nerve had been injured, and there was no other episode of right eye

problem other than in 1993. Id.

In a follow-up visit to Dr. Hamdi in January 2000, he again notes that petitioner’s fundus

was normal on the left but atrophied on the right. Id. On three separate occasions, Dr. Hamdi

noted that petitioner’s optic nerve on the right was pale or atrophied and that she had optic

neuritis in 1993. Id. Petitioner had no other eye problems between 1993 and 2000 so that one

could say she had optic neuritis after 1993 (but not in 1993) which was not recognized. Tr. at 37.

Seeing pallor in the optic nerve depends on where the inflammation is. Tr. at 38. If the

inflammation is further back than the retinal part of the optic nerve, it could take several years

before one sees the sequelae of that inflammation. Id.

Petitioner returned to Dr. Hamdi on December 17, 1999 (Ex. 17, p. 10) with sudden onset

of loss of vision in her left eye, decreased visual acuity, burning sensations, and hyperaesthesias

in both lower extremities, which mean she had an acute problem. Tr. at 39. But, on

examination, petitioner did not have any relative afferent pupillary defect, meaning that she was

in that group of people who did not have a change in her pupils when she had optic neuritis. Id.

12

Dr. Tornatore did not believe that petitioner had retinopathy or central serous retinopathy

in 1993 when she had a leaking blood vessel. Tr. at 40. To diagnose petitioner in 1993, Dr.

Hrisomalos used the code 362.63 (Ex. 4, p. 5) for lattice degeneration. Id. That indicates myopia

in the very fringes of the eye where the retina is pulled a bit. Id. Dr. Tornatore doubts that

petitioner had a retinal or a myopic problem for just one time. Tr. at 41. A few months later,

petitioner had all the symptoms to diagnose MS. Id. These included the symptoms of optic

neuritis. It would not make sense for her to have retinal detachment and then optic neuritis. Id.

Dr. Hrisamolos should have examined petitioner’s pupils and he did not. Tr. at 42. Dr. Hamdi

felt that what happened in 1993 was optic neuritis. Id.

Comparing the symptoms of petitioner in 1993 in the right eye with her symptoms in

1999 in the left eye, Dr. Tornatore stated that in 1993, she had decreased acuity as if she had a

screen in front of her eye, but in 1999, she had sudden loss of vision. Tr. at 43. The basic

symptoms for 1993 and 1999 were loss of or change of vision in one eye that occurred relatively

suddenly. Id. On June 28, 1993, petitioner’s vision in her right eye was 20/60. Tr. at 45. The

same was for the left eye. Id. On August 2, 1993, petitioner’s vision in her right eye was 20/80,

and in her left 20/50, showing some changes in both eyes. Id. In optic neuritis, patients typically

have reduced visual acuity ranging from nearly normal to no light perception, citing to Ex. 23.

Tr. at 46. One does not have to have complete loss of vision to have optic neuritis. Id. In

reduced visual acuity, the sharpness of vision is reduced. Id.

Dr. Tornatore’s opinion is that petitioner’s onset of MS occurred within a month of her

third hepatitis B vaccination. Tr. at 47. His basis is his interpretation of petitioner’s visit to Dr.

Hrisomalos in June 1993, her symptoms, and Dr. Hamdi’s 1999 concurrence that petitioner had

13

optic neuritis in 1993. Dr. Hamdi was petitioner’s treating neurologist. Id. Dr. Tornatore

connects petitioner’s onset of optic neuritis one month after her third hepatitis B vaccination with

her subsequent diagnosis of MS three months later. Id. His basis is that optic neuritis is an

inflammatory autoimmune disease of the optic nerve which is frequently the heralding symptom

of someone who is going to develop MS. Tr. at 47-48. The percentage of patients who have

optic neuritis and subsequently develop MS is very high. Tr. at 48.

On cross-examination, Dr. Tornatore admitted that headache, sparklers (photopsias), a

veil-like film over the eyes, and color change can be symptoms of a retinal disorder. Tr. at 50.

Petitioner had some lattice degeneration at the periphery of her retina. Tr. at 51. But changes at

the periphery would not entail changes throughout the eye such as the screen. Id. Dr. Tornatore

questioned why if petitioner had retinal detachment, she did not continue to have this as a

problem. Tr. at 52. Patients with high myopia such as petitioner are at high risk for retinal

detachment. Tr. at 53-54.

Dr. Tornatore stated that Dr. Hamdi gave us the piece of information six years later when

he wrote that he saw petitioner’s right disk was atrophied and pale, and that she had optic neuritis

in 1993. Tr. at 54. Dr. Hamdi said that because no eye problem intervened between 1993 and

1999. Id.

Dr. Aaron Miller testified for respondent. Tr. at 56. He is a neurologist specializing in

MS. Tr. at 58. His opinion is that it is extremely improbable that petitioner had optic neuritis in

June 1993. Tr. at 59. Petitioner lacked all the common symptoms of optic neuritis in June 1993.

Id. The symptoms she had are more likely related to retinal disease. Id. The hallmark of her

complaints was photopsias or sparklers. Tr. at 59-60. Her symptoms in 1999 comprised the

14

hallmarks of optic neuritis when she saw Dr. Hamdi, who made the appropriate diagnosis of

optic neuritis, i.e., loss of vision in one eye that occurs suddenly and is usually accompanied by a

scotoma which is like a hole in the field of vision. Tr. at 60. Pain frequently accompanies it

when the eye moves. In the aftermath, people with optic neuritis have an afferent pupillary

defect. Id. But petitioner never had an afferent pupillary defect in her right eye. Id. Dr. Miller

admitted on questioning from the undersigned that petitioner did not have an afferent pupillary

defect in her left eye when Dr. Hamdi saw her. Id.

Dr. Miller stated he had seen hundreds of patients with optic neuritis and cannot recall

anyone complaining of sparklers or photopsias. Tr. at 60-61. Patients with optic neuritis tell him

they lost vision in one eye or their vision in one eye is very blurry, often with pain on eye

movement. Tr. at 61. On examination, he may or may not see optic pallor. The inflammation is

frequently behind the optic nerve preventing the examiner from seeing acute inflammation. Id.

Dr. Sermersheim, the neurologist who diagnosed petitioner in September 1993 with MS,

specifically looked at her pupils and did not note an afferent pupillary defect. Tr. at 61-62. He

also did not note any optic atrophy which was at least three full months after petitioner’s initial

visual symptoms. Tr. at 62.

Dr. Hrisomalos in 1993 found a number of abnormalities in petitioner’s retina:

photopsias, flashing lights, sparklers. They are far more typical of retinitis. Id. Petitioner did

not have any of the hallmarks of optic neuritis in June 1993: sudden or rapid loss of vision,

afferent pupillary defect, scotoma. Id. Her visual acuity was the same in both eyes. Id.

Dr. Miller stated he was not surprised that Dr. Hamdi found pallor indicating atrophy in

petitioner’s right optic nerve in 1999 and that finding did not indicate she had a bout of optic

15

neuritis in 1993. Tr. at 63, 64. Acute optic neuritis means an episode in which symptoms of

acute inflammation occur: loss of vision, very blurry unilateral vision, a hole in the field of

vision, pain on movement, resulting in the loss of myelin. Tr. at 63. This results ultimately in

the pallor of the disk. Id. A lot of MS patients will have damage to their optic nerve insidiously

over time without an acute episode. It is not uncommon to find them with an afferent pupillary

defect in one eye when they never noticed symptoms. Id. Dr. Miller believes that petitioner’s

optic atrophy which Dr. Hamdi noticed in 1999 in petitioner’s right optic nerve occurred after the

time Dr. Sermersheim examined petitioner’s optic nerves in September 1993 and did not notice

optic atrophy and before 1999 when Dr. Hamdi examined petitioner’s eyes. Tr. at 64-65.

Dr. Miller stated that, in June 1993, petitioner did not have loss of visual acuity, afferent

pupillary defect, pallor of the optic nerve, or a scotoma. Tr. at 65-66. He admitted on cross-

examination that a patient with loss of visual acuity will most typically complain of blurred

vision in one eye. Tr. at 67. Petitioner did complain her vision was blurred, as if she were

looking through a screen in front of her eye. Id. Dr. Miller admitted that complaining of looking

through a screen could be a symptom of optic neuritis. Id. But petitioner in June 1993 had no

difference in the visual acuity between her two eyes. Tr. at 68. In the second visit, in August

1993, she had lower visual acuity in the right eye than in the left. Id. A very small percent of

patients with optic neuritis have no change in visual acuity. Id. There was a difference of 20

points between the first and second eye examinations (June and August 1993). Tr. at 69. Dr.

Miller’s experience is that patients with optic neuritis do not complain about flashing lights. Tr.

at 70. He disagreed with Dr. Tornatore that a retinal problem would not have gone away. Dr.

Miller testified that retinal problems can be intermittent. Tr. at 71.

16

Dr. Miller agreed that color changes can be a symptom of optic neuritis. Id. A washing

out of color is a very common manifestation of optic neuritis. Tr. at 72. Someone looking at the

retina would also be looking at the optic nerve. Id. He thinks it ridiculous that Dr. Hrisomalos

would not have commented on petitioner’s optic nerve if he had seen anything abnormal about it

in 1993. Tr. at 73. He agreed that if the inflammation was further down the optic nerve,

someone would not see it on examination by just looking at the retina. Tr. at 73-74. It usually

takes a few months to develop atrophy after optic neuritis. Tr. at 74. It might take longer than

from June to September 1993 to develop atrophy, but Dr. Miller said an afferent pupillary defect

should be present from the beginning. Id. However, Dr. Miller agreed that petitioner never had

afferent pupillary defect in either eye. Id.

Dr. Miller disagrees with Dr. Hamdi’s diagnosis of bilateral optic neuritis, because the

“itis” implies an active inflammatory process. Tr. at 74-75. Dr. Miller prefers to say that

petitioner had bilateral optic neuropathy, i.e., a disease of both optic nerves. Tr. at 75. Dr. Miller

thinks it was inappropriate for Dr. Hamdi to assume that what he observed in petitioner’s eye in

1999 was the result of optic neuritis in 1993 when the person examining petitioner in 1993 did

not diagnose that. Tr. at 76. Petitioner denied having had any visual symptoms at all in

September 1993 when she saw Dr. Sermersheim. Tr. at 77.

Upon questioning from the undersigned, Dr. Tornatore stated that three months between

the time petitioner saw Dr. Hrisomalos in June 1993 and Dr. Sermersheim in September 1993

was a relatively short time to start to develop optic atrophy in her right eye since her degree of

inflammation of that optic nerve was not great. Tr. at 77-78. If there were an insidious

inflammation, it would take longer. Tr. at 78.

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In answer to the undersigned’s question, Dr. Miller stated that Dr. Hamdi in 1999 would

not have known when petitioner’s optic neuritis in her right eye began and therefore there was no

reason for him to assume she had optic neuritis in 1993. Tr. at 80. He thinks there is no clear

evidence that petitioner ever had acute optic neuritis in her right eye. She did have it in her left

eye in 1999. Tr. at 82. She had optic neuropathy, not neuritis, in her right eye because Dr.

Hamdi observed pallor or atrophy of her optic disk, implying that at some point over the years

she had damaged the right optic nerve. Tr. at 82-83.

Dr. Tornatore thought that petitioner had optic neuritis, not neuropathy, on June 28, 1993.

Tr. at 85. It came on in the course of a week meaning something abrupt happened. This

indicates an acute inflammatory process rather than slow smoldering, but it was not bad because

her visual acuity was 20/60 in June 1993. Id. One-quarter of optic neuritis patients do not have

afferent pupillary defect. Id.

Dr. Miller agreed that petitioner’s visual acuity improved to 20/20 bilaterally without

correction. Tr. at 86. He does not doubt that petitioner had optic neuritis in her left eye in 1999

when she had MS. Tr. at 88. She never had an afferent pupillary defect in either eye. Tr. at 88-

89.

DISCUSSION

This is a causation in fact case. To satisfy her burden of proving causation in fact,

petitioner must offer "(1) a medical theory causally connecting the vaccination and the injury; (2)

a logical sequence of cause and effect showing that the vaccination was the reason for the injury;

and (3) a showing of a proximate temporal relationship between vaccination and injury.” Althen

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v. Secretary of HHS, 418 F. 3d 1274, 1278 (Fed. Cir. 2005). In Althen, the Federal Circuit

quoted its opinion in Grant v. Secretary of HHS, 956 F.2d 1144, 1148 (Fed. Cir. 1992):

A persuasive medical theory is demonstrated by “proof of a logical sequence ofcause and effect showing that the vaccination was the reason for the injury[,]” thelogical sequence being supported by “reputable medical or scientificexplanation[,]” i.e., “evidence in the form of scientific studies or expert medicaltestimony[.]”

In Capizzano v. Secretary of HHS, 440 F.3d 1274, 1325 (Fed. Cir. 2006), the Federal

Circuit said “we conclude that requiring either epidemiologic studies, rechallenge, the presence

of pathological markers or genetic disposition, or general acceptance in the scientific or medical

communities to establish a logical sequence of cause and effect is contrary to what we said in

Althen....”

Close calls are to be resolved in favor of petitioners. Capizzano, 1440 F.3d at 1327;

Althen, 418 F.3d at 1280. See generally, Knudsen v. Secretary of HHS, 35 F.3d 543, 551 (Fed.

Cir. 1994).

Without more, "evidence showing an absence of other causes does not meet petitioners'

affirmative duty to show actual or legal causation." Grant, 956 F.2d at 1149. Mere temporal

association is not sufficient to prove causation in fact. Id. at 1148.

Petitioner must show not only that but for the vaccine, she would not have had optic

neuritis and MS, but also that the vaccine was a substantial factor in bringing about her optic

neuritis and MS. Shyface v. Secretary of HHS, 165 F.3d 1344, 1352 (Fed. Cir. 1999).

The Federal Circuit in Capizzano emphasized that the special masters are to consider

seriously the opinions of petitioner’s treating doctors. In that case, four of petitioner’s treating

doctors opined that hepatitis B vaccine caused her rheumatoid arthritis. 440 F.3d at 1326.

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In Werderitsh v. Secretary of HHS, No. 99-310V, 2006 WL 1672884 (Fed. Cl. Spec.

Mstr. May 26, 2006), the undersigned ruled that hepatitis B vaccine can cause MS and did so in

that case. Petitioner’s transient monocular visual symptoms in her right eye were suggestive of

optic neuritis and occurred several days to a week after her first hepatitis B vaccination. 2006

WL 1672884, at *19. She had symptoms of transverse myelitis a month after her second

vaccination, and was diagnosed with MS. Respondent’s expert, Dr. Roland Martin, testified that

the appropriate onset interval, if a vaccination were to cause an acute reaction, would be a few

days to three to four weeks. Stevens v. Secretary of HHS, No. 99-594V, 2006 WL 659525, at

*15 (Fed. Cl. Spec. Mstr. Feb. 24, 2006).

Both experts in the instant action are neurologists specializing in MS. Both agree that

petitioner had optic neuritis. Both experts also agree that optic neuritis is frequently the hallmark

of MS. Their difference is in attributing the optic pallor or atrophy in petitioner’s right eye to

either optic neuritis (according to Dr. Tornatore with onset in June 1993) or to optic neuropathy

(according to Dr. Miller with onset some time between 1993 and 1999 when Dr. Hamdi,

petitioner’s treating neurologist, noted the pallor in petitioner’s right optic nerve when she had

come to him with symptoms of optic neuritis in her left eye).

One of Dr. Miller’s reasons for doubting that petitioner had optic neuritis in her right eye

when Dr. Hrisomalos saw her in June 1993 was the absence of an afferent pupillary defect in her

right eye. But he agrees that petitioner had optic neuritis in her left eye in 1999 when petitioner

did not have an afferent pupillary defect in her left eye. Therefore, Dr. Miller accepts that in an

MS patient, the patient may have optic neuritis without an afferent pupillary defect, as the

literature shows is the case with a minority of optic neuritis patients. It lessens Dr. Miller’s

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credibility for him to deny petitioner had optic neuritis in her right eye in 1993 because of the

absence of an afferent pupillary defect when that sign was equally missing from her left eye in

1999 when he agrees she had optic neuritis. This point of the defense was not well-considered.

Whereas Dr. Tornatore interprets petitioner’s June 1993 complaints of sparkles, a film

over her eye, blurry vision, and headache as indicative of optic neuritis, Dr. Miller interprets

these symptoms as symptoms of retinal problems. But petitioner never had a retinal problem

again. Both doctors agreed that these symptoms could be consistent with optic neuritis as the

literature shows. Petitioner also experienced less visual acuity and her eyes had disparate acuity

in her next visit to Dr. Hrisamolos in August 1993.

The tie-breaker in this case must be the opinion of petitioner’s treating neurologist Dr.

Hamdi who, in 1999, when petitioner came to him complaining of undisputed optic neuritis in

her left eye, diagnosed her with having had optic neuritis in her right eye in 1993 after he

examined her eyes and found pallor in her right optic nerve. The symptoms about which she

complained in June 1993 to Dr. Hrisomalos, although consistent with a retinal problem, are also

consistent with optic neuritis. As Dr. Tornatore stated, and Dr. Miller agreed, if the

inflammation were further back in her eye, Dr. Hrisomalos, and later Dr. Sermersheim, a

neurologist who diagnosed petitioner with MS in September 1993, would not have seen the

inflammation. Optic neuritis is inflammation of the optic nerve.

The Federal Circuit in Capizzano emphasized taking into serious consideration the

opinions of petitioner’s treating doctors. There is no reason to doubt Dr. Hamdi’s diagnosis after

evaluating petitioner’s eyes that her right optic nerve pallor or atrophy was due to a prior optic

neuritis in 1993, the only time that she voiced visual complaints before 1999.

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It seems an extraordinary stretch to adopt Dr. Miller’s opinion that some time after

petitioner saw Dr. Sermersheim in September 1993 but before she saw Dr. Hamdi in 1999, she

had a smoldering inflammatory process which did not reach the acuteness of optic neuritis but

did cause her right optic nerve to atrophy and yet ignore totally her complaints of sparkles, blurry

or filmy vision, and screened vision in June 1993 which stayed the same or worsened when she

saw Dr. Hrisomalos again in August 1993. Dr. Hamdi reached his opinion before there was any

litigation. He was her treating neurologist. Dr. Tornatore’s opinion is consistent with Dr.

Hamdi’s diagnosis and the undersigned accepts it as accurate. Because petitioner’s optic neuritis

was not severe, both eyes recovered 20/20 visual acuity. But this does not negate the occurrence

of petitioner’s earlier right eye optic neuritis, even though it was relatively mild.

Since petitioner’s onset of right optic neuritis was within a month of her third hepatitis B

vaccination, the onset is medically appropriate for causation. In Werderitsh, petitioner also had

optic neuritis before her diagnosis of MS. The undersigned discussed in Werderitsh the

biologically plausible medical theory connecting hepatitis B vaccine and MS. 2006 WL

1672884, at *24-*26. The undersigned notes that Althen concerned the onset of optic neuritis

two weeks after tetanus toxoid vaccination followed by the demyelinating disease acute

disseminated encephalomyelitis. 418 F.3d at 1281.

Each expert in the instant case agrees that optic neuritis is frequently a hallmark for MS.

There is a logical sequence of cause and effect connecting petitioner’s exposure to hepatitis B

vaccine and her onset of demyelinating disease. Petitioner has proved causation in fact.

CONCLUSION

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Petitioner is entitled to reasonable compensation. The undersigned hopes that the parties

may reach an amicable settlement, and will convene a telephonic status conference soon to

discuss how to proceed in resolving the issue of damages.

IT IS SO ORDERED.

October 31, 2008 s/ Laura D. Millman DATE Laura D. Millman

Special Master

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